Role of renal hemodynamics and arterial pressure in aldosterone "escape".

Hall, John E.; Granger, J. P.; Smith, M. J.; Premen, A. J.

doi:10.1161/01.hyp.6.2_pt_2.i183

Cited by 129 publications

(75 citation statements)

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“…In a 9-yr follow-up study, we showed that primary aldosteronism is characterized by partially reversible renal dysfunction (20), and demonstration that albuminuria is a marker of a hemodynamic rather than a structural renal defect has been reported also by Ribstein et al (19) in a short-term, postadrenalectomy evaluation of patients with adrenal adenoma. In agreement with the findings of studies that were conducted in more experimental settings (37)(38)(39), longitudinal studies consistently demonstrate that the hallmark of renal dysfunction in primary aldosteronism is reversible glomerular hyperfiltration that contributes to increase urinary albumin losses.…”

Section: Discussionsupporting

confidence: 84%

Relationships of Plasma Renin Levels with Renal Function in Patients with Primary Aldosteronism

Catena¹,

Colussi²,

Nadalini³

et al. 2007

Clinical Journal of the American Society of Nephrology

102

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Background: The renal damage that is present in primary aldosteronism might reflect functional and potentially reversible abnormalities that are initiated by glomerular hyperfiltration. The aim of this study was to investigate the relationships of plasma renin and aldosterone concentrations with renal outcomes after treatment of primary aldosteronism.Design, setting, participants, and measurements: Fifty-six consecutive patients who had primary aldosteronism and were recruited in a university center were studied. Patients were prospectively followed after either surgical or medical treatment for a mean of 6.2 yr, during which they received antihypertensive drugs to reach a target BP of <140/90 mmHg.Results: At baseline, patients with primary aldosteronism had higher creatinine clearance and albuminuria than 323 patients with essential hypertension and 113 normotensive individuals. In patients with primary aldosteronism, plasma active renin levels that were higher than the lower limit of detection (2.5 pg/ml) were associated with higher BP, plasma potassium, and albuminuria and lower creatinine clearance. Plasma aldosterone concentrations that were higher than the median value (225 pg/ml) were associated with lower plasma potassium and higher creatinine clearance. Creatinine clearance was correlated directly with plasma aldosterone and inversely with renin. During follow-up, patients with higher baseline plasma renin required use of more antihypertensive drugs to obtain BP control and had a smaller early decline in albuminuria than did patients with suppressed renin.Conclusions: Escape of renin from suppression by excess aldosterone is associated with evidence of more severe renal damage in patients with primary aldosteronism and predicts less favorable outcomes after treatment.

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Section: Discussionsupporting

confidence: 84%

Relationships of Plasma Renin Levels with Renal Function in Patients with Primary Aldosteronism

Catena¹,

Colussi²,

Nadalini³

et al. 2007

Clinical Journal of the American Society of Nephrology

102

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“…17 Furthermore, it was shown that the infusion of aldosterone for 1 week to normotensive dogs determined a 20% to 24% increase of GFR, which was associated with an increase of renal perfusion pressure. 34 However, in the present study, GFR was slightly higher in PH than in PA patients with APA and IHA, both when raw and when covariate-adjusted GFR values were compared. Furthermore, we found a weak inverse significant relation (rϭϪ0.135; PϽ0.001) of GFR with UAE rate at univariate correlation, although this was not significant at multivariate analysis.…”

Section: Uae Rate In Pa and Ph Patientscontrasting

confidence: 69%

Renal Damage in Primary Aldosteronism

et al. 2006

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Abstract-Primary aldosteronism (PA) has been associated with cardiovascular hypertrophy and fibrosis, in part independent of the blood pressure level, but deleterious effects on the kidneys are less clear. Likewise, it remains unknown if the kidney can be diversely involved in PA caused by aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA). Hence, in the Primary Aldosteronism Prevalence in Italy (PAPY) Study, a prospective survey of newly diagnosed consecutive patients referred to hypertension centers nationwide, we sought signs of renal damage in patients with PA and in comparable patients with primary hypertension (PH). Patients (nϭ1180) underwent a predefined screening protocol followed by tests for confirming PA and identifying the underlying adrenocortical pathology. Renal damage was assessed by 24-hour urine albumin excretion (UAE) rate and glomerular filtration rate (GFR). UAE rate was measured in 490 patients; all had a normal GFR. Of them, 31 (6.4%) had APA, 33 (6.7%) had IHA, and the rest (86.9%) had PH. UAE rate was predicted (PϽ0.001) by body mass index, age, urinary Na ϩ excretion, serum K ϩ , and mean blood pressure. Covariate-adjusted UAE rate was significantly higher in APA and IHA than in PH patients; there were more patients with microalbuminuria in the APA and IHA than in the PH group (Pϭ0.007). Among the hypertensive patients with a preserved GFR, those with APA or IHA have a higher UAE rate than comparable PH patients. Thus, hypertension because of excess autonomous aldosterone secretion features an early and more prominent renal damage than PH. Key Words: hypertension, endocrine Ⅲ aldosterone Ⅲ mineralocorticoids Ⅲ kidney Ⅲ hypertrophy Ⅲ adrenal gland T he results of large intervention trials 1,2 and cross-sectional studies (reviewed by Rossi et al 3 ) have recently refueled the interest on the deleterious cardiovascular effects of excess aldosterone. Moreover, growing evidence 4 indicates that primary aldosteronism (PA) is a common cause of secondary hypertension: in the Primary Aldosteronism Prevalence in Italy (PAPY) study, a prospective survey of 1180 consecutive newly diagnosed hypertensive patients referred to specialized hypertension centers, aldosterone-producing adenoma (APA) and idiopathic hyperaldosteronism (IHA) were found in 4.8% and 6.4% of all patients, respectively, thus leading to an overall prevalence of PA of Ϸ11%. 5 It has been contended that this form of secondary hypertension is relatively "benign," that is, devoid of cardiovascular complications, because of the suppression of the renin-angiotensin system, which plays a substantial role in cardiovascular remodeling and damage. 6,7 This view has, however, been challenged by recent data. 3,8 PA has in fact been associated with widespread tissue fibrosis, 9 vascular remodeling, 10 and excess prevalence of left ventricular hypertrophy and diastolic dysfunction 11 that were corrected by adrenalectomy. 12 A higher incidence of cardiovascular complications, including atrial fibrillation, has also been...

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“…DOCA salt is a "prototype" model for salt-sensitive hypertension. 4 Secondary renin-angiotensin-aldosterone system suppression, 5 increased secretion of natriuretic peptides, 6 and altered pressure natriuresis 7 establish a new steady state between Na ϩ intake and Na ϩ excretion at a new blood pressure level. The kidneys escape the mineralocorticoid signal, and additional salt retention ceases, albeit with increased blood pressure.…”

mentioning

confidence: 99%

Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

et al. 2006

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Abstract-Water-free Na ϩ storage may buffer extracellular volume and mean arterial pressure (MAP) in spite of Na ϩ retention. We studied the relationship among internal Na ϩ , K ϩ , water balance, and MAP in Sprague-Dawley rats, with or without deoxycorticosterone-acetate (DOCA) salt, with or without ovariectomy (OVX). The rats were fed a low-salt (0.1% NaCl) or high-salt (8% NaCl) diet for 5 weeks. DOCA salt increased MAP (161Ϯ14 versus 123Ϯ4 mm Hg; PϽ0.05), and DOCA-OVX salt increased MAP further (181Ϯ22 mm Hg; PϽ0.05). DOCA salt increased the total body Na ϩ by Ϸ40% to 45%; however, water-free Na ϩ retention by osmotically inactive Na ϩ storage and by osmotically neutral Na ϩ /K ϩ exchange allowed the rats to maintain the extracellular volume close to normal. DOCA-OVX salt rats showed similar Na ϩ retention. However, their osmotically inactive Na ϩ storage capacity was greatly reduced and only partially compensated by neutral Na ϩ /K ϩ exchange, resulting in greater volume retention despite similar Na ϩ retention. For every 1% wet weight total body water gain, MAP increased by 2.3Ϯ0.2 mm Hg in DOCA salt rats and 2.5Ϯ0.3 mm Hg in DOCA-OVX salt rats. Because water-free Na ϩ retention buffered total body water content by 8% to 11% wet weight, we conclude that this internal Na ϩ escape buffered MAP. Extrarenal Na ϩ and volume balance seem to play an important role in long-term volume and MAP control. Key Words: electrolytes Ⅲ gender Ⅲ water-electrolyte balance Ⅲ hypertension, sodium-dependent S alt sensitivity describes a reproducible relationship between increasing salt intake and blood pressure. 1 Blood pressure may increase because of increased cardiac output, increased peripheral resistance, or both. Volume-dependent and volume-independent factors contribute. Volumeindependent factors include autonomic nerve activity and molecules that modulate peripheral vascular resistance and heart muscle work. Volume-dependent aspects are based on extracellular fluid volume (ECV). Na ϩ is the major extracellular cation that osmotically acts to hold ECV water; the total body Na ϩ (TBNa ϩ ) has become synonymous for volume regulation. 2,3 Deoxycorticosterone-acetate (DOCA) decreases renal Na ϩ excretion and increases TBNa ϩ and total body volume. DOCA salt is a "prototype" model for salt-sensitive hypertension. 4 Secondary renin-angiotensin-aldosterone system suppression, 5 increased secretion of natriuretic peptides, 6 and altered pressure natriuresis 7 establish a new steady state between Na ϩ intake and Na ϩ excretion at a new blood pressure level. The kidneys escape the mineralocorticoid signal, and additional salt retention ceases, albeit with increased blood pressure. 8 We showed recently that DOCA rats given 1% saline accumulated 4.75 mmol Na ϩ . 9 Only 20% of this Na ϩ load exerted osmotic activity and led to water retention, whereas the rest accumulated as water free by osmotically inactive Na ϩ storage and/or osmotically neutral Na ϩ /K ϩ exchange. In Sprague-Dawley rats, we found that ovariectomy (OVX) reduced th...

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Role of renal hemodynamics and arterial pressure in aldosterone "escape".

Cited by 129 publications

References 0 publications

Relationships of Plasma Renin Levels with Renal Function in Patients with Primary Aldosteronism

Relationships of Plasma Renin Levels with Renal Function in Patients with Primary Aldosteronism

Renal Damage in Primary Aldosteronism

Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

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Role of renal hemodynamics and arterial pressure in aldosterone "escape".

Cited by 129 publications

References 0 publications

Relationships of Plasma Renin Levels with Renal Function in Patients with Primary Aldosteronism

Relationships of Plasma Renin Levels with Renal Function in Patients with Primary Aldosteronism

Renal Damage in Primary Aldosteronism

Extrarenal Na + Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats

Contact Info

Product

Resources

About

Extrarenal Na ⁺ Balance, Volume, and Blood Pressure Homeostasis in Intact and Ovariectomized Deoxycorticosterone-Acetate Salt Rats